Epoxyeicosatrienoic acids and heme oxygenase-1 interaction attenuates diabetes and metabolic syndrome complications

Prostaglandins Other Lipid Mediat. 2012 Jan;97(1-2):1-16. doi: 10.1016/j.prostaglandins.2011.10.002. Epub 2011 Nov 15.


MSCs are considered to be the natural precursors to adipocyte development through the process of adipogenesis. A link has been established between decreased protective effects of EETs or HO-1 and their interaction in metabolic syndrome. Decreases in HO-1 or EET were associated with an increase in adipocyte stem cell differentiation and increased levels of inflammatory cytokines. EET agonist (AKR-I-27-28) inhibited MSC-derived adipocytes and decreased the levels of inflammatory cytokines. We further describe the role of CYP-epoxygenase expression, HO expression, and circulating cytokine levels in an obese mouse, ob/ob(-/-) mouse model. Ex vivo measurements of EET expression within MSCs derived from ob/ob(-/-) showed decreased levels of EETs that were increased by HO induction. This review demonstrates that suppression of HO and EET systems exist in MSCs prior to the development of adipocyte dysfunction. Further, adipocyte dysfunction can be ameliorated by induction of HO-1 and CYP-epoxygenase, i.e. EET.

Publication types

  • Review

MeSH terms

  • 8,11,14-Eicosatrienoic Acid / metabolism*
  • Animals
  • Diabetes Complications / metabolism*
  • Diabetes Complications / pathology
  • Diabetes Complications / physiopathology
  • Heme Oxygenase-1 / metabolism*
  • Humans
  • Metabolic Syndrome / complications*
  • Metabolic Syndrome / metabolism
  • Metabolic Syndrome / pathology
  • Metabolic Syndrome / physiopathology
  • Protein Binding


  • Heme Oxygenase-1
  • 8,11,14-Eicosatrienoic Acid